All publications referenced herein are incorporated by reference to the same extent as if each publication or patent application was specifically and individually indicated to be incorporated by reference. The following description includes information that may be useful in understanding the present invention. It is not an admission that any of the information provided herein is prior art or relevant to the presently claimed invention, or that any publication specifically or implicitly referenced is prior art.
The Human Microbiome Project (HMP) is improving our understanding of the dynamics of microbiota in healthy individuals, and the pathogenic capabilities of key species that mediate poor health outcomes (1,2). Understanding the molecular mechanisms that mediate symbiosis between commensal bacteria and humans may redefine how we view the evolution of adaptive immunity and consequently how we approach the treatment of numerous immunologic disorders. The skin is one of five anatomic locations studied as part of the HMP. The molecular composition of this organ is derived from host cells, microbiota, and external molecules. The chemical makeup of the skin surface is largely undefined. Recently, Bouslimania et al. developed 3D maps revealing that the molecular composition of skin has diverse distributions and that the composition is defined not only by skin cells and microbes but also by daily routines, including the application of hygiene products (3).
The composition of the human skin microbiota has been correlated with skin anatomy, dividing into moist, dry, and sebaceous microenvironments, and can be influenced by beauty and hygiene (3). The skin is our first line of defense against foreign invaders and is also home to a diverse population of microbes. The majority of these microbes are commensal (nonpathogenic permanent residents) or transient (temporary residents) organisms. In pathogenic interactions, only the microbe benefits, while the host is eventually harmed. Many skin pathogens can be typically found living on the skin as commensal organisms, but microbial dysbiosis (or microbial imbalance), host genetic variation, and immune status may drive the transition from commensal to pathogen (4).
Analysis of bacterial diversity on human skin employing 16S rRNA gene sequencing revealed that multiple skin sites exhibited greater bacterial diversity than in the gut and oral cavity; interpersonal variation varied significantly within the population studied, and the temporal stability of the analyzed skin microbial communities remained relatively stable (5). Physiological characteristics of various skin sites are associated with different levels of bacterial diversity (6). Spatially, the skin microbiota may extend to subepidermal compartments (7). Regions such as the face, chest, and back, areas with a high density of sebaceous glands, promote growth of lipophilic microorganisms such as Propionibacterium and Malassezia. 
It is postulated that the predominant fungus of the skin microbiota, Malassezia, is involved in seborrhoeic dermatitis. This chronic inflammatory skin disorder is often first diagnosed around puberty and is caused by an increase in cutaneous lipids resulting from androgen-driven sebaceous gland development and sebum secretion (8). The disease also often occurs in patients older than 50 years. Dandruff is the common term for seborrhea of the scalp. It is mainly associated with M. restricta and M. globosa (9,10), and has a very high prevalence of nearly 50% of the population (8). Improvements in the disease can be achieved by therapeutic application of antifungal, but not antibacterial agents. The mechanisms underlying pathogenicity are incompletely understood. Impaired skin barrier function facilitates the course of the disease (11). The fungus secretes a lipase that splits triglycerides into irritant fatty acids that may induce hyperproliferation and scaling, or releases arachidonic acid, which is also involved in inflammation (12). From the current literature it can be speculated that the fungus, which is part of the normal skin microbiota, switches to a pathogenic state when its growth is not controlled. What these control factors are and how they are dampened are not yet understood.